Neonatal hypocalcemia and hyperphosphatemia occur in a significant number of premature infants, infants with birth asphyxia, and infants of diabetic mothers. Based on our clinical work defining the incidence and pattern of change of serum and urinary Ca, P and Mg in these 3 groups of infants we plan to further define the pathophysiologic mechanisms in neonatal hypocalcemia. Our previous work suggests that hypomagnesemia, increased urinary calcium losses and unresponsiveness to parathyroid hormone are not the causes of neonatal hypocalcemia. We plan to examine the hypotheses that maternal hyperparathyroidism, fetal hypercalcemia, neonatal hypoparathyroidism and endogenous neonatal phosphate loading are the cause of neonatal hypocalcemia. Radioimmunoassay of maternal and neonatal serum parathyroid hormone levels, serum ionized calcium levels and urinary cyclic AMP concentrations will be specifically studied. The results of these studies will provide knowledge of the basic mechanisms in neonatal Ca, P, Mg and parathyroid hormone homeostasis. The basic understanding of such mechanisms will provide a logical basis for prevention and therapy of neonatal hypocalcemia.